During the last few years we found that antibodies against the negative charged azobenzene-arsonate residue (As) are expressed predominantly in the a1 and a2 allotypes of heterozygous rabbits of the allotypes a1, 3 or 2, 3; very little anti-As antibody of the allotype a3 is formed. The same rabbits produce large amounts of anti-BSA and anti-TMA of all three allotypes a1,a2, and a3 (BSA eauals bovine serum albumin, TMA equals azobenzene-N-trimethylammonium) when injected with As-TMA-BSA. While our results on the a1, 3 heterozygotes have been published, those with the a1, 2 and a2, 3 allotypes need confirmation by quantitative analyses in a larger number of animals. Ingraham and Chien in our medical school in Indianapolis found the same low expression of the a3 allotype in the heterozygotes of the allotype a1, 3 injected with azobenzene-sulfonate-BSA. The great influence of negatively or positively charged groups on the allotype of the induced antibodies suggests that the antigen interferes directly with the formation of antibody molecules from their precursors, the heavy (H) and light (L) peptide chains, i.e., with a phenotypic reaction. I proposed therefore that the antigen acts as a stereo-specific co-factor which first combines non-covalently with those free H-chains which either fit closely to the antigenic determinants or carry groups of the opposite charge. The antigen would thus activate these selected H chains for the formation of the disulfide (SS) bonds with suitable L chains. I intend to test this view by means of isotopically labeled antigen molecules. Some of these experiments can be performed in my laboratory. Others may involve methods for which we are not equipped here. I may then have to ask other investigators in our Biology group or elsewhere for their cooperation. My views on the mechanism of antigen-induced antibody formation have been published in the May issue 1978 of the Proceedings of the National Academy of Sciences.